Feline spongiform encephalopathy

Feline spongiform encephalopathy (FSE) is a disease that affects the brains of felines. It is caused by proteins called prions.[1] FSE is thought to be related or identical to bovine spongiform encephalopathy (BSE).[2][3] This disease is known to affect domestic and captive feline species.[4] This infectious agent might be spread by both haematogenous and nervous pathways.[5] Like BSE, this disease can take several years to develop. It is probable, but not proven, that the affected animals contract the disease by eating contaminated bovine meat.[6]

Symptoms and signs[edit]

Clinical signs of FSE typically develop gradually in housecats. Initial signs of the condition include behavioral changes such as aggression, timidity, and hiding. Other commonly observed motor signs include gait abnormalities and ataxia, which typically affect the hind legs first. Affected cats may also display poor judgement of distance, and some cats may develop a rapid, crouching, hypermetric gait. Another common symptom is hyperesthesia. Some affected cats may exhibit an abnormal head tilt, tremors, a vacant stare, excessive salivation, decreased grooming behaviors, polyphagia, polydipsia, and dilated pupils. Once signs of FSE appear, the disease progresses and results in death within a few weeks to 3 months.[7]

Ataxia was observed to last for about 8 weeks in the affected animals. The ultimate result is death of the infected animals.[2]

Diagnosis[edit]

This disease can only be confirmed at the post-mortem, which includes identification of bilaterally symmetrical vacuolation of the neuropil and vacuolation in neurones. Lesions are likely to be found in basal ganglia, cerebral cortex and thalamus of the brain.[citation needed]

Treatment[edit]

This is a terminal condition and there is currently no specific treatment for the disease.[2]

Epidemiology[edit]

This disease was first reported in domestic cats within the United Kingdom in 1990.[8][4] Since 1990, cases have been reported in other countries and other feline species in captivity, although most affected felines originated in the UK.[9]

References[edit]

  1. ^ Iulini, B.; Cantile, C.; Mandara, M. T.; Maurella, C.; Loria, G. R.; Castagnaro, M.; Salvadori, C.; Porcario, C.; Corona, C.; Perazzini, A. Z.; Maroni, A.; Caramelli, M.; Casalone, C. (September 2008). "Neuropathology of Italian cats in feline spongiform encephalopathy surveillance". Veterinary Pathology. 45 (5): 626–633. doi:10.1354/vp.45-5-626. PMID 18725465.
  2. ^ a b c "Feline spongiform encephalopathy (FSE)". Provet Healthcare Information. October 2013. Retrieved 2020-02-29.
  3. ^ Bencsik, Anna; Debeer, Sabine; Petit, Thierry; Baron, Thierry; Mabbott, Neil (7 September 2009). "Possible case of maternal transmission of feline spongiform encephalopathy in a captive cheetah". PLOS ONE. 4 (9): e6929. Bibcode:2009PLoSO...4.6929B. doi:10.1371/journal.pone.0006929. PMC 2732902. PMID 19738899.
  4. ^ a b Eiden, M.; Hoffmann, C.; Balkema-Buschmann, A.; Muller, M.; Baumgartner, K.; Groschup, M. H. (21 July 2010). "Biochemical and immunohistochemical characterization of feline spongiform encephalopathy in a German captive cheetah". Journal of General Virology. 91 (11): 2874–2883. doi:10.1099/vir.0.022103-0. PMID 20660146.
  5. ^ Lezmi, Stephane; Bencsik, Anna; Monks, Eoin; Petit, Thierry; Baron, Thierry (1 May 2003). "First case of feline spongiform encephalopathy in a captive cheetah born in France: PrPsc analysis in various tissues revealed unexpected targeting of kidney and adrenal gland". Histochemistry and Cell Biology. 119 (5): 415–422. doi:10.1007/s00418-003-0524-5. PMID 12783238. S2CID 38376121.
  6. ^ "Mad Cow Disease and Cats". College of Veterinary Medicine, Cornell University. 15 Nov 2006.
  7. ^ "Feline Spongiform Encephalopathy" (PDF). Center for Food Security and Public Health. Retrieved 27 February 2023.
  8. ^ "ARCHIVE: BSE: Other TSEs". Archived from the original on 2012-08-17. Retrieved 2012-09-02.
  9. ^ Imran, Muhammad; Mahmood, Saqib (1 November 2011). "An overview of animal prion diseases". Virology Journal. 8 (1): 493. doi:10.1186/1743-422X-8-493. PMC 3228711. PMID 22044871.


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